GADD153 Blocking Peptide
- Known as:
- GADD153 Blocking Peptide
- Catalog number:
- 33r-10755
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- GADD153 Blocking Peptide
Related genes to: GADD153 Blocking Peptide
- Gene:
- DDIT3 NIH gene
- Name:
- DNA damage inducible transcript 3
- Previous symbol:
- -
- Synonyms:
- CHOP10, GADD153, CHOP
- Chromosome:
- 12q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-11
- Date modifiied:
- 2016-10-05
Related products to: GADD153 Blocking Peptide
Related articles to: GADD153 Blocking Peptide
- New half-sandwich iridium(III) compounds [Ir(η-Cp)Cl(L1-3)]PF (-), combining Cp* or Cp with N,P-coordinated phosphinoalkylamines L1-L3, were tested in different cancer cells (2D and 3D cultures), including MOR/CPR cisplatin-resistant lung carcinoma. Best-performing compound outperformed its Cp analogue and cisplatin in MOR/CPR cells while sparing noncancerous cells. Multiomics profiling shows a non-DNA-targeted mechanism: rapid integrated stress response with ER stress (DDIT3/CHOP) and oxidative stress (HMOX1, ATF3), nucleolar stress, and primary inhibition of ribosome biogenesis and mitochondrial translation. These changes drive translational shutdown, suppression of oxidative phosphorylation with a glycolytic shift, and G arrest, alongside endolysosomal remodeling (enhanced vesicular uptake, reduced degradative capacity) that favors intracellular retention. The phenotype is predominantly cytostatic with apoptotic priming. In vivo, suppressed tumor growth and activated apoptosis with low systemic toxicity. Compound thus emerges as a promising prototype Ir(III) metallodrug that disrupts nucleolar, mitochondrial, and lysosomal homeostasis to overcome resistance. - Source: PubMed
Publication date: 2026/06/16
Štarha PavelFriedecká JaroslavaHéžová RenataBárta OndřejJarošová ReaMašek JosefNemec IvanMilde DavidNovobilský AdamNovotný LadislavOndruš JaroslavŠterbinská SlavomíraStraková NicolLenobel RenéHošek Jan - Typhimurium (. Typhimurium) is an enteric pathogen that employs a variety of mechanisms to exploit inflammation, resulting in expansion in the intestinal tract, but host factors that contribute to or counteract the luminal expansion are not well-defined. Endoplasmic reticulum (ER) stress induces inflammation and plays an important role in the pathogenesis of infectious diseases. However, little is known about the contribution of ER stress-induced inflammation during pathogenesis. Here, we demonstrate that the ER stress markers and are induced in the colon of . Typhimurium-infected mice, but the pro-apoptotic transcription factor which encodes the protein CHOP, is significantly reduced. . Typhimurium-infected mice deficient for CHOP displayed a significant decrease in inflammation, colonization, dissemination, and pathology compared to littermate control mice. Preceding the differences in . Typhimurium colonization, a significant decrease in gene and inducible nitric oxide (NO) synthase (iNOS) protein expression was observed. Deletion of decreased the bioavailability of nitrate in the colon, leading to a reduced fitness advantage of wild-type . Typhimurium over a mutant strain (deficient in nitrate respiration). CD11b CCR2 myeloid cells, but not intestinal epithelial cells, produced iNOS, resulting in nitrate bioavailability for . Typhimurium to expand in the intestinal tract in a CHOP-dependent manner. Altogether, our work demonstrates that the host protein CHOP facilitates iNOS expression in CD11b CCR2 cells, thereby contributing to luminal expansion of . Typhimurium via nitrate respiration.IMPORTANCE Typhimurium is a gastroenteric bacterium that replicates to large numbers within the gastrointestinal (GI) tract, allowing for efficient host-to-host transmission. One strategy that allows to expand in the GI tract is via nitrate respiration that is generated during infections. The host protein CHOP is activated within the unfolded protein response (UPR), an adaptive response pathway that is activated when cells are undergoing endoplasmic reticulum (ER) stress. ER stress has been implicated in several infectious and inflammatory diseases; however, little is known about the contribution of ER stress and the UPR during infections. Our results presented here provide more insight into the role of CHOP in the production of nitrate and the subsequent growth of in the GI tract. Altogether, our research provides a better understanding of the contribution of the ER stress protein CHOP in intestinal health and disease. - Source: PubMed
Publication date: 2026/06/15
Alexander Elizabeth ASweet Lydia AKuss-Duerkop Sharon KByndloss Mariana XSchaberg Tamarah EKeestra-Gounder A Marijke - Gliomas are highly aggressive brain tumors that pose significant challenges in terms of prognosis and treatment. The precise expression patterns and prognostic significance of necroptosis-related genes (NRGs) in gliomas remain poorly understood, despite necroptosis demonstrating promise as a therapeutic target in cancer. - Source: PubMed
Publication date: 2026/06/11
Wu KaixiangCao LuYang HongchuanSun WenwenWu Kaifu - Cancer and depression frequently co-occur, leading to a poor prognosis. Circadian rhythm disruption is a contributing factor, yet its precise role in the development of this comorbidity remains to be illustrated. - Source: PubMed
Publication date: 2026/06/04
Tang LianshaDu YilingLiu SiyiHuang YunqiHe WenboHu HandanWang JiayaoLiu JiyanWang Qiang - Keratoconus (KCN) is a bilateral and asymmetric cornea disease. Autophagy plays an important role in homeostasis by protecting cells against stress. However, the roles of autophagy-related genes (ARGs) in KCN remains unclear. Hence, this study aimed to identify the signatures of ARGs of KCN and explore their correlation with immune infiltration. Transcriptional data and clinical information of patients with KCN were downloaded from the profile data GSE112155 and GSE151631. Functional analysis was used to reflect the biological functions, and weighted gene co-expression network analysis was applied to excavate co-expression modules of autophagy-related expression patterns. Moreover, gene set enrichment and variation analyses were performed for pathway analysis. Consensus clustering analysis was used to cluster different molecular subtypes on the basis of gene expression profiles of KCN-specific ARGs. Single-sample gene set enrichment analysis was employed to calculate separate enrichment scores for each immunocyte between KCN and healthy samples. Finally, hub genes were verified by real-time quantitative polymerase chain reaction. We first identified 14 ARGs differentially expressed between patients with KCN and controls using NetworkAnalyst. Nine overlapped genes (BNIP3, CDKN1A, DDIT3, FOS, HSPA5, MAPK8IP1, MYC, PPP1R15A, and VEGFA) (P < .05) were identified using a random forest model. The MAPK signaling pathway, apoptosis, FoxO signaling pathway, and protein processing in endoplasmic reticulum signaling were mainly involved. The weighted gene co-expression network analysis classified the genes into 12 distinct modules. The MEturquoise (correlation = 0.51), MEpink (correlation = 0.535) were significantly positively correlated with KCN, whereas the MEyellow (correlation = -0.776) and MEgreen (correlation = -0.664) were negatively correlated. Single-sample gene set enrichment analysis showed a close interaction between immune cell infiltration and the development of KCN. Finally, all the 9 hub genes except VEGFA were significantly downregulated (P < .05) using real-time quantitative polymerase chain reaction. We described the signatures of ARGs in KCN, the distribution of immune cells between KCN patients and the control, and the correlation between hub genes related to autophagy and KCN disease. This demonstrates the potential roles of autophagy mechanisms and the immune response in KCN, providing a novel insight into understanding the pathogenesis of KCN and potential treatment targets. - Source: PubMed
Li SutongWang GangChen JingLi Naiyang